ArticleLearning & memory (Cold Spring Harbor, N.Y.)2015
16p11.2 Deletion mice display cognitive deficits in touchscreen learning and novelty recognition tasks.
Article in Learning & memory (Cold Spring Harbor, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
44 citing papers in PubMed, 71 citations in OpenAlex.
- A simple method that doubles learning speed for mice in touchscreen-based visual discrimination.Scientific reports · 2025Article
- Investigate the differences in executive functions and behavioral baseline indicators of Parkinson's disease model mice based on the five - choice serial reaction time task.Laboratory animal research · 2025Article
- Atrial fibrillation-induced neurocognitive and vascular dysfunction is averted by mitochondrial oxidative stress reduction.JCI insight · 2025Article
- 16p11.2 duplication shows early male-biased impacts on reward learning, but NMDA receptor antagonism reduces optimal choice selection in both wildtypes and 16p11.2 duplication.bioRxiv : the preprint server for biology · 2025Article
- The "don't eat me" signal CD47 is associated with microglial phagocytosis defects and autism-like behaviors in 16p11.2 deletion mice.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Poly (I:C)-induced maternal immune activation generates impairment of reversal learning performance in offspring.Journal of neurochemistry · 2025Article
- Understanding copy number variations through their genes: a molecular view on 16p11.2 deletion and duplication syndromes.Frontiers in pharmacology · 2024Review
- Sleep disturbances in autism spectrum disorder: Animal models, neural mechanisms, and therapeutics.Neurobiology of sleep and circadian rhythms · 2023Review
- Critical periods and Autism Spectrum Disorders, a role for sleep.Neurobiology of sleep and circadian rhythms · 2023Article
- Visiomode: An open-source platform for building rodent touchscreen-based behavioral assays.Journal of neuroscience methods · 2023Article
- Histone Deacetylase Inhibition Restores Behavioral and Synaptic Function in a Mouse Model of 16p11.2 Deletion.The international journal of neuropsychopharmacology · 2022Article
- Touchscreen cognitive deficits, hyperexcitability and hyperactivity in males and females using two models of Cdkl5 deficiency.Human molecular genetics · 2022Article
- Social behavior in 16p11.2 and 22q11.2 copy number variations: Insights from mice and humans.Genes, brain, and behavior · 2022Review
- Impact of Intestinal Microbiota on Cognitive Flexibility by a Novel Touch Screen Operant System Task in Mice.Frontiers in neuroscience · 2022Article
- Computational identification of variables in neonatal vocalizations predictive for postpubertal social behaviors in a mouse model of 16p11.2 deletion.Molecular psychiatry · 2021Article
- Sex-Specific Stress-Related Behavioral Phenotypes and Central Amygdala Dysfunction in a Mouse Model of 16p11.2 Microdeletion.Biological psychiatry global open science · 2021Article
- Reversal of synaptic and behavioral deficits in a 16p11.2 duplication mouse model via restoration of the GABA synapse regulator Npas4.Molecular psychiatry · 2021Article
- Deletion of a non-canonical regulatory sequence causes loss of Scn1a expression and epileptic phenotypes in mice.Genome medicine · 2021Article
- Translational outcomes relevant to neurodevelopmental disorders following early life exposure of rats to chlorpyrifos.Journal of neurodevelopmental disorders · 2020Article
- Overexpression of astroglial major histocompatibility complex class I in the medial prefrontal cortex impairs visual discrimination learning in mice.Molecular brain · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Chromosomal 16p11.2 deletion syndrome frequently presents with intellectual disabilities, speech delays, and autism. Here we investigated the Dolmetsch line of 16p11.2 heterozygous (+/-) mice on a range of cognitive tasks with different neuroanatomical substrates. Robust novel object recognition deficits were replicated in two cohorts of 16p11.2+/- mice, confirming previous findings. A similarly robust deficit in object location memory was discovered in +/-, indicating impaired spatial novelty recognition. Generalizability of novelty recognition deficits in +/- mice extended to preference for social novelty. Robust learning deficits and cognitive inflexibility were detected using Bussey-Saksida touchscreen operant chambers. During acquisition of pairwise visual discrimination, +/- mice required significantly more training trials to reach criterion than wild-type littermates (+/+), and made more errors and correction errors than +/+. In the reversal phase, all +/+ reached criterion, whereas most +/- failed to reach criterion by the 30-d cutoff. Contextual and cued fear conditioning were normal in +/-. These cognitive phenotypes may be relevant to some aspects of cognitive impairments in humans with 16p11.2 deletion, and support the use of 16p11.2+/- mice as a model system for discovering treatments for cognitive impairments in 16p11.2 deletion syndrome.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.